Figure 1.
Model, left part: LSCs are enriched in the ROS low fraction of AML blasts. ROS low cells maintain a higher basal autophagy flux compared ROS high cells. Right part: Genetic or pharmacological inhibition of autophagy triggered a p53 dependent apoptotic response in p53 wild type AMLs, which is severely dampened in TP53 mutant AMLs.

Model, left part: LSCs are enriched in the ROS low fraction of AML blasts. ROS low cells maintain a higher basal autophagy flux compared ROS high cells. Right part: Genetic or pharmacological inhibition of autophagy triggered a p53 dependent apoptotic response in p53 wild type AMLs, which is severely dampened in TP53 mutant AMLs.

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